Musculoskeletal Flashcards
List enzymes which indicates myonecrosis, the time to peak serum concentration following muscle damage, their half lives and tissues they are found in.
- Creatine kinase (CK): peaks within 4-6h; moderate elevations decrease to normal range in 24-48h; cardiac and skeletal muscle.- Aspartate transaminase (AST): peak at 24h; half life weeks; muscle, red blood cell, liver, other tissues. - Lactate dehydrogenase (LDH): peak at 15h.
What test can you perform to identify subclinical rhabdomyolysis in horses?
- Exercise stress test.- 15 minutes exercise: trot/walk unfit horses, steady trot fit horses; blood sample pre and 4-6 hours post-exercise.- Normal horse: CK elevates within 3 x normal range.- Rhabdomyolysis: greater than 5 x CK elevation.
Describe normal and abnormal findings following electromyography in the horse
- Normal muscle shows burst of activity following needle insertion then quiescence (little spontaneous elec activity unless the horse moves).- Horse with abnormalities in elec condition system of muscle or denervation of endplate show abnormal spontaneous activity e.g. fibrillation potentials, positive sharp waves. - Myopathic changes incl decrease in duration and amplitude of motor unit action potentials.
What are the main features and two types of myotonias found in horses.
- Delayed relaxation of muscle after mechanical stimulation or voluntary contraction.- Abnormal muscle membrane excitability shared feature.1. Non-dystrophic myotonias: myotonia congenita, HYPP.2. Dystrophic myotonia: progressive dz.
Describe the signalment of horses most commonly affected by shivers.
- Breeds: Draught horse breed, WBs, WB x, TBs.- Age: > 1yo.- Gender: male > female.- Height: >16.3hh.
What is aetiology of shivers?
- Unknown. Proposed aetiologies incl genetic, traumatic, infectious and neurologic diseases.- No abnormalities on electromyography, indicating it is not a true myotonic condition.
Describe the clinical signs of shivers.
- Primarily affects the HLs.- Characterised by periodic, involuntary spasms of the muscles in the pelvic region, pelvic limbs and tail which are exacerbated by backing or picking up the HLs.- HL in elevated, abducted and tailhead usually elevates concurrently and trembles.
Describe the clinical signs and aetiology of myotonia congenita in horses.
- Signs manifest in first year of life and do not progress beyond 6-12 months of age.- Well developed musculature with bilateral bulging/dimpling of the thigh and rump muscles.- Stimulation exacerbates muscle dimpling and affected muscles may remain contracted for a minute or more.- Mild to mod pelvic limb lameness; gait abnormalities improve with exercise.- Genetic mutation identified in one New Forrest Pony w congenital myotonia: autosomal recessive c.1775A>C mutation –> substitution of aspartic acid for alanine in codon 592 of the CLCN1 protein.
Describe the clinical signs of myotonia dystrophica and the breeds in which it has been reported.
- Severe clinical signs of myotonia that progress to marked muscle atrophy and possibly involve a variety of organs.- Retinal dysplasia, lenticular opacities and gonadal hypoplasia have been reported in 1 QH foal.- Reported in QHs, Appaloosas and Italian-bred foals.
How is a diagnosis of myotonia made?
- Tentative dx on the basis of age and CSx.- Definitive dx: electromyography –> pathognomonic, crescendo-decrescendo, high-frequency repetitive bursts with characteristic dive-bomber sound.- Muscle biopsy histo: myotonia congenita may be normal or may demonstrate very variable type I muscle fibre dimension up to twice normal; myotonic dystrophy: ringed fibres, alterations in the shape and position of myonuclei, sarcoplasmic masses and an inc in endomysial and perimysial connective tissues, type II and II involved.
What is the prognosis for horses with myotonia?
- Tx recommendations not possible; two reports of QH w HYPP and myotonic dystrophy responding to phenytoin.- Px variable and dependent on severity of CSx.- Mildly affected may show amelioration of signs w age.- Severely affected may have progression requiring euth.
Describe the aetiology of equine hyperkalaemic periodic paralysis (HYPP) and breeds affected by this disorder.
- Autosomal dominant trait.- Point mutation that results in a phenylalanine/leucine substitution in a key part of the voltage-dependent skeletal muscle sodium channel alpha subunit.- QHs, American Paint Horses, Appaloosas and QH x.
Describe the pathophysiology of HYPP.
- Mutation in voltage-dependent skeletal muscle sodium channel alpha subunit –> resting membrane potential is closer to firing than in normal horses.- The HYPP mutation results in a failure of a subpopulation of Na+ channels to inactivate when serum-K+ concentrations are inc (excessive K+ intake or exercise followed by rest) –> excessive inward flux of Na+ and outward flux of K+ –> persistent depolarisation of muscle cells and temporary weakness.
List the clinical signs of HYPP.
- Range from asymptomatic to daily muscle fasicultations and weakness.- CSx develop by 2-3yo; normal between episodes.- CSx precipitated by high dietary K+ intake (>1.1%) e.g. alfalfa hay, molasses, elec supplements, kelp-based supplements; fasting, anaesthesia or heavy sedation, trailer rides, stress; exercise per se does not stimulate signs.- Myotonia: prolapsed nictitans, muscle fasiculations, become more generalised, exacerbated by stimulation.- Sweating.- Muscular weakness, may result in recumbency.- Horses may be tachycardic, tachypnoeic, anxious.- Dypsnoea or dysphagia, URT collapse, laryngeal paralysis.- Episodes last for 15-60mins; may cause death.
How do you diagnose a horse with HYPP?
- Descent from sire Impressive + CSx suggestive.- Demonstrate base-pair sub in the abnormal segment of DNA encoding for the alpha subunit of the Na+ channel.- Electromyography: abnormal fibrillation potentials, complex repetitive discharges, occasional myotonic potentials, trains of doublets between episodes.- During episode CBC/MBA: hyperkalaemia (6-9mmol/L), haemoconcentration, mild hyponatraemia, n A-B balance.
Outline the treatment which can be administered to horses with HYPP during a clinical episode.
- Mild episode: mild exercise or giving oral corn syrup or grain to stimulate insulin-mediated intraceullar mvt of K+.- Adrenaline IM (3ml of 1:1000/500Kg).- Acetazolamide 3mg/kg PO q8-12h.- Calcium gluconate 0.2-0.4ml/kg of 23% solution in 1L 5% dextrose –> inc extracellular Ca++ –> inc muscle membrane potential –> dec membrane hyperexcitability.- Dextrose 6mg/kg 5% solution +/- sodium bicarbonate 1-2mEq/kg –> enhanced intracellular movement of K+.- Tracheostomy if severe respiratory obstruction.
Outline the treatment which can be administered to horses with HYPP between episodes to try and reduce their occurrence.
- Decrease dietary K+: feed 0.6-1.1% K+ in inc K+ excretion; acetazolamide also stabilised blood glucose and K+ by stim insulin secretion.
What is the prognosis for horses with HYPP?
In most cases manageable, but may be recurrent or fatal.
What species of clostridial organisms have been isolated from large animals with clostridial myonecrosis?
- Chauvoei, septicum, sordelli commonly.- Occasionally novyi type B, perfringens type A, carnis.- Mixed infections common.
List the clinical signs of clostridial myonecrosis.
- Commonly rapidly progressive with development of tremors, ataxia, dyspnoea, recumbency, coma and death within 12-24h.- Severe depression.- Fever.- Tachypnoea.- Anorexia.- Swollen muscles; usually inj site horse, usually trunk/legs and sometimes mm around vulva, tongue, diaphragm, udder in ruminants.- Skin over muscles initially hot, swollen, discoloured –> cool, insensitive, sloughs +/- crepitus.- Discharge/aspiration = malodorous serosanguinous.
List diagnostic test findings in patients with clostridial myositis.
- CK and AST elevated; often not indicative of severity.- CBC/MBA consistant w toxaemia e.g. haemoconcentration, leukocytosis, toxic changes.- Cytology of aspirate: gram positive, spore-forming rod.- Tissue samples for direct smears, fluorescent antibody testing and anaerobic bacterial culture –> organism.
Describe the pathophysiology of clostridial myonecrosis.
- Clostridial organisms ubiquitous in the environment.- Route of entry unknown but suspected to be direct inoculation (wound or inj) or GIT –> liver and skeletal muscle as dormant spores.- Tissue devitalisation (inj, transport, herding, handling) –> spores germinate –> rapid vegetative process –> release of exotoxins –> muscle necrosis and toxaemia.- Exotoxins vary depending on clostridial species involved; necrotising (lecithinase) and haemolysing (haemolysin) toxins appear to be of greatest importance.- C. sordelli toxins most potent –> fatal myositis.
Describe the epidemiology of clostridial myonecrosis in horses.
- Associated w puncture wounds and IM injection sites.- IM irritating drugs implicated e.g. antihistamines, anthelmintics, phenylbutazone, flunixin meglumine.
Describe the necropsy findings in animals that have died from clostridial myonecrosis.
- Rapid swelling and autolysis.- Bloodstained discharge from body orifices.- Engorgement of the subcutis and adj tissues with bloodstained tissue and gas bubbles.- Muscles firm, moist at periphery, lighter, drier in centre.- Odour like rancid butter.- Lungs often congested; fibrinohaemorrhagic pleuritis. - Heart, spleen and liver often friable.- C. sordelli: death often so rapid s/c gas accum is rare; see local myonecrosis, subendocardial haemorrhages in left ventricle, haemorrhage in trachea, bronchi, thymus, renal calyces; perirenal oedema, severe lung congestion.
Outline the prognosis and treatment of clostridial myonecrosis.
- Px guarded to poor, often fatal; C. perfringens better Px.- AB: 44,000 IU/kg penicillin q2-4h until stable (1-5d) then swap to q6h or change to oral metronidazole.- Agressive surgical debridement incl fasciotomy.- Supportive care: IVFT, NSAIDs, ice boots.
Define muscle cramps vs muscle contractures and list aetiologies of the two.
- Muscle cramps: arise from hyperactivity of motor units caused by repetitive firing of the peripheral and/or central nervous system; induced by forceful contraction of a shortened muscle, changes in ECF electrolyte composition (low Na, low K, diet, endurance exercise) and ear ticks.- Muscle contractures: painful spasms that represent a state of muscle contracture unaccompanied by depolarisation of the muscle membrane; malignant hyperthermia and some forms of exertional myopathies.
Describe the presentation and treatment of ear-tick associated muscle cramping.
- Infestation with Otobius megnini (ear ticks).- Intermittent signs of severe muscle cramping of pectoral, triceps, abdominal or semimem/semitend lasting from minutes to hours.- Stimulation/percussion –> myotonic cramp, fall over.- CK elevated at 4,000-170,000 IU/L.- Local tx of ticks with pyrethrins and piperonal butoxide –> recovery in 12-23h.- Acepromazine may help with muscle cramps.
Describe the clinical presentation of acute rhabdomyolysis associated with Streptococcus equi.
- Reported in QHs firm, swollen, panful epaxial and gluteal muscles –> recumbency.- Unrelenting pain necessitating euth w/in 24-48h.
List clinicopathologic abnormalities reported in horses with acute rhabdomyolysis associated with Streptococcus equi.
- Mature neutrophilia.- Hyperfibrinogenaemia.- Marked elevations in CK 115,000-587,000 U/L.- Marked elevations in AST 600-14,500 U/L.- Titres to SeM protein are low (unless recently vaccinated).- Titres to myosin binding protein high in small number of horses tested.
List necropsy findings reported in horses with acute rhabdomyolysis associated with Streptococcus equi.
- Large pale areas of necrotic mm. in HL and lumbar mm.- Histo: severe acute myonecrosis with a degree of macrophage infiltration.- Sublumbar muscles more severe and chronic necrosis.
What is the proposed aetiology of Streptococcus equi associated rhabdomyolysis?
- Toxic shock-like reaction arising from profound T-cell stimulation by streptococcal superantigens with the release of high levels of inflammatory cytokines.2. Bacteraemia with local multiplications and production of exotoxins or proteases within skeletal muscle.
Outline treatment and prognosis for horses with acute rhabdomyolysis associated with Streptococcus equi.
- Tx w IV penicillin once CSx of strangles and myopathy –> high mortality rate.- Aggressive early tx may be successful.- Rifampin (inhibits protein synth) + penicillin.- Flush GPs and drain abscesses to dec bacterial load.- NSAIDs and high doses of short-acting corticosteroids may dec inflammatory response.- Manage pain: lignocaine, detomidine, ketamine CRI.- Deep bedding, turn q4h, sling if possible.
List the incidence and inciting causes of infarctive purpura haemorrhagica.
- Severe form of purpura with high fatality rate; one study 3/53 cases of purpura.- Exposure to S. equi within 3 weeks of presentation.- Vaccination for S. equi.- Concurrent Salmonella infantum infection.- Titres for SeM protein may be markedly elevated.
List clinical signs of infarctive purpura haemorrhagica in horses.
- Painful lameness with limb swelling, muscle stiffness.- +/- colic.- Petechiae.- Oral infarctions resembling ulcers.- Moderate well-demarcated limb oedema.- Local, firm intramuscular swellings.- +/- dec borborygmi and haemorrhagic gastric reflux.
List potential diagnostic test abnormalities in horses with infarctive purpura haemorrhagica.
- Leukocytosis.- Neutrophilia with left shift and toxic changes.- Hyperproteinaemia.- Markedly elevated CK 47,000-280,000 U/L.- Markedly elevated AST 960-7,000 U/L.- Immune complexes in serum primarily composed of IgM or IgA and streptococcal M protein.- Peritoneal fluid: WNL or inc TP, NCC and RBCC.- U/S: focal hypoechoic lesions within muscle tissue.- Biopsies: palpable normal muscles WNL; swollen muscles: acute coagulative necrosis.
List post mortem findings in horses with infarctive purpura haemorrhagica.
- Infarction of skeletal muscles, skin, GIT, pancreas and lungs.- S. equi abscessation of a lymph node.- Histo: leukocytoclastic vasculitis and acute coagulative necrosis resembling infarction in numerous tissues.
Outline treatment and prognosis for horses with infarctive purpura haemorrhagica.
- High fatality rate.- Early recognition and aggressive tx nec for survival.- Penicillin, NSAIDs, tapering steroids over months.
What is the typical signalment of horses with immune-mediated polymyositis (IMM)? Are there any triggering factors?
- QH bloodlines.- 16yo.- 1/3 of cases have had exposure of S. equi or resp dz.
What is the most prominent clinical sign of IMM?
- Rapid onset of muscle atrophy, particularly affecting the back and croup muscles, accomp by stiffness and malaise.- Atrophy may involve 50% of muscle mass in 1wk.
List potential diagnostic test abnormalities in horses with IMM.
- CK/AST: WNL or mild to moderately elevated.- Biopsy of epaxial and gluteal muscles: lymphocytic vasculitis, angular atrophy, lymphocyte myofibre infiltration, fibre necrosis with macrophage infiltration and regen.- Biopsy of semimem/semitend: may show evidence of atrophy or vasculitis but inflamm infiltrates may be absent.- Inflamm infiltrates in muscle samples contain high CD4:CD8 ratio w no evidence of IgG binding to myofibres.
Outline treatment and prognosis for horses with IMM.
- If concurrent evidence of S. equi infection tx w ABs.- Tapering steroids over 1 month.- Avoid IM injections.- Muscle mass gradually recovers over 2-3mo.- Recurrence of atrophy is common and may require additional corticosteroid therapy.- Some horses develop residual muscle atrophy.
List viruses implicated in development of virus-associated myopathy and the muscle groups affected.
- Muscle necrosis represents component of multiple organ system involvement.- Myocarditis: FMD, EI, EIA.- Myocarditis or skeletal muscle myositis: bovine ephemeral fever, MCF, BVD, bluetongue.- Primary muscle stiffness: EI, EHV-1.
Cysts of the sporozoan parasite Sarcocystis are commonly found in the heart, oesophagus and skeletal muscle of cattle, sheep, goats and horses. What clinical signs are seen with experimental heavy infestations?
- Fever.- Anaemia - extravascular haemolysis and haemorrhage into many tissues.- Chronic myositis.- Muscle wasting/decreased gain.- Sometimes death.- Hair loss on the rump, neck and tail.- Abortion in sheep and goats.
Describe the lifecycle of Sarcocystis in different large animal species.
- Carnivores = definitive host; herbivores = intermediate host - ingested carnivore faeces.- Cattle IH: S. cruzi (Canidae), S. hirsuta (Felidae), S. hominis (primates).- Horse IH: S. bertrami, S. equicanis, S. fayeri (dogs).- Sheep IH: S. ovicanis (Canidae).- Goats IH: S. capracanis (Canidae).
How do you diagnose sarcocystosis?
History, clinical signs, elevated muscles enzymes, immature cysts in muscle biopsies.
How do you control and treatment sarcocystosis in large animals?
- Control: prevent feed contamination w carnivore faeces.- Cattle: ionophores may prevent.- Tx only likely successful if very early.- Tx: ionophore ABs or amprolium in food animals; successful tx in one horse w TMS, pyremethamine and phenylbutazone was reported.
Describe the aetiology and presentation of masseter muscle myodegeneration in horses.
- Adult horses with selenium deficiency normal or MMM.- Acute bilateral swelling of masseter muscles, trismus, dysphagia and salivation.- Necropsy: histo evidence of bilateral symmetric lesions in masseters and muscles of FLs and HLs.- Tachycardias, arrhythmias may indicate myocardial damage.- Inc CK, AST, elevated CTn, pigmenturia.- Guarded Px but some reports of successful tx w enteral nutrition, IVFT, IM Se and oral vit E.- Without tx may –> permanent trismus due to muscular atrophy and fibrosis.
Describe the presentation and outcome of vitamin E-deficient myopathy.
- CSx of EMND, deficiency in vit E, lacking evidence of neurogenic atrophy in the sacrocaudalis dorsalis (but does have moth-eaten staining pattern of mitochondria)- Muscle a-tocopherol conc low, serum conc variably low.- Muscle weakness could be reversible manifestation of sk m mitochondrial oxidative stress assoc w vit E defic.- Horses can recover completely w 5000IU/d vit E q >3 wk.- Could be entity to itself or predecessor to dev of EMND.
List toxic causes of rhabdomyolysis.
- Ionophores: – Susceptibility: horses>sheep>pigs>goats>cattle.– Rhabdomyolysis and cardiomyopathies.– Incl monensin, lasolacid, naracin, salinomycin, laidlomycin.- Inj of lignocaine, diazepam, digoxin, levamisole, nitroclofene, pentazocine, thiazinamium, chloro, oxytet, ivermectin.- Organophosphate toxicosis.- Blister beetle toxicity (rarely).- Tetrachlorovinphos mini ponies (fly control agent).- Gossypol: monogastrics should not ingest feed w >200ppm gossypol, mature ruminants tolerate 20g/head/day.- Cassia (sicklepod), Eupatorium rugosum (white snakeroot), Isocoma wrightii (rayless goldenrod) –> cardiomyopathy and skeletal muscle degen; tremetone active in dried/dead plants.
What is the aetiology of malignant hyperthermia in the horse?
- Genetic mutation in the ryanodine receptor 1 (RYR1) gene –> excessive Ca++ release from the sarcoplasmic reticulum.- QH and paints.
Describe clinical presentation of a 6wk old Arabian cross foal with suspected congenital centronuclear myopathy.
- Normal at birth and first month of life.- Generalised weakness and muscle atrophy.- Only able to stand for 15-20mins w short, choppy gait.- Electromyography: dec insertional activity, fibrillation potentials, positive sharp waves, and complex repetitive discharges in all of the muscles examined. Amplitudes of the motor unit action potentials were subjectively dec.- Muscle histo: excessive variability in myofiber size, fibers with centrally located nuclei; electron microscopy: numerous vacuoles filled with granular debris consistent with dilatation of the t-tubular system and triads, z-line disruption and myofibrillar disarray; consistent w CNM in other spp.- Supportive care through several hospital visits but found dead in stall at 5mo of age.Ref: J. Vet. Intern. Med. 2014;28(6):1886–1891.
Describe clinical presentation and evidence of myocardial dysfunction in an Arabian mare with masseter myodegeneration.
- 22yo Arabian mare w 2d Hx dysphagia, salivation and bilateral swelling of the masseter muscles.- Good appetite but masseters swollen and painful and mastication ineffective; HR 60bpm, PE otherwise WNL.- CBC WNL, elevated muscle and liver enzymes, marked pigmenturia, Se conc undetectable, Vit E conc WNL.- U/S: masseter mm thickened, increased muscle echogenicity and patchy blurring of the fasciae within the muscle layers = inflammation and oedema.- Tx: PBZ, dexamethasone, IM Vit E/Se, oral Vit E and methocarbabol, IV CRIs lignocaine and medetomidine –> CSx improved over week but persistent tachycardia.- 24-h Holter ECG: sinus tachycardia with sporadic supraventricular and uniform ventricular dysrhythmias, cTnI = 11.6ng/mL (ref bilateral mm atrophy; gradually able to chew and swallow and cardiac function n; discharged on day 17 on Vit E/Se, masseter mm WNL at 6mo.Ref: J. Vet. Intern. Med. 2011; 25(5):1171–1180.
Describe the clinical signs of congenital myotonia in goats.
- ‘Fainting goats’.- CSx recognisable by 6wks of age; remain throughout life but not progressive.- Vary from stiffness after rest to marked general rigidity after visual, tactile or auditory stimulation.
What is the aetiology of congenital myotonia in goats?
Autosomal dominant mutation in the skeletal muscle chloride channel (CLCN1) that has incomplete penetrance.
Describe the epidemiology of clostridial myonecrosis in sheep and goats.
- Most frequently associated with wounds occurring after shearing, docking and unsanitary surgical procedures.- Inc risk if dipped for parasites after shearing if dip becomes contaminated with clostridial spores.
Describe the aetiology of hypokalaemic myopathy in dairy cattle.
- Occurs when serum K+ concentrations are
List the clinical signs of hypokalaemic myopathy in dairy cattle.
- Severe weakness.- Recumbency.- Abnormal position of the head and neck.- Rumen hypomotility or atony.- Abnormal faeces.- Anorexia.- Tachycardia.
List diagnostic test findings in dairy cattle with hypokalaemic myopathy.
- Serum K+
Outline the treatment of hypokalaemic myopathy in dairy cattle.
- Tx difficult as serum K+ conc do not necessarily reflect muscle K+ conc.- KCl IV 16g/100Kg - do not exceed 0.5mEq/kg/h.- KCl PO 26-42/100Kg - do not exceed 230g PO q12h.- Tx to resolve primary cause of ketosis and anorexia.
What is the prognosis for survival in dairy cattle with hypokalaemic myopathy?
22-79%.
Describe the epidemiology of clostridial myonecrosis in cattle.
- Cattle: 4-24mo; young colostral ABs, older acquired IR.- Animals on high planes of nutrition in excellent body condition most likely to develop dz.- C. sordelli most common in older feedlot cattle.- C. chauvoei most common in warm weather; spring to fall.- C. septicum, C. novyi and C. perfringens type A usually assoc w skin wounds e.g. inj sites, punctures, castration.- Infections in genital area can occur post-dystocia.
Outline a vaccination program for prevention of clostridial myonecrosis in cattle.
- Multivalent bacterin toxoids containing antigens against multiple clostrididial spp incl chauvoei, septicum, novyi, sordelli, perfringens.- Initial vacc at 4-6mo, repeat, then q6-8mo.- Usually only nec up to 3yo but continue if high-risk area.
